Pathogen Protein Driven Calcium Channel Activation at the Root of MECFS?

Remy

Administrator
I struggled with where to put this post. And I struggled with the title too. For those of you that know me, or have been following my posts for a while, you probably know that I've been sick for about 7 years now. My first bout of illness was following mono in my senior year of high school. After that, my illness waxed and waned (but mostly waned) through my 20s until I was hit by a motorcycle crossing the street one night on my way home. Then it was a long 8 year downward stretch into the mostly housebound state I find myself in today.

Over the course of the past 7 years, I've basically tried everything available to me in terms of meds and supplements (except Rituximab because I'm not yet convinced that's the answer). Antivirals and antibiotics, IV and oral and every supplement known to man practically. And while I've made some improvements, I'm still not *better*.

I give this backstory so that my waffling on the cause of MECFS makes more sense...I've gone from being certain it was a pathogen of some sort, probably herpes family, to being certain it was Lyme disease, to being certain it was mold, to finally being certain it was just the immune system gone haywire and reacting spectacularly to everything even when nothing was there anymore.

And now I'm leaning back towards a viral pathogen at the heart of the immune system insanity.

So here goes nothing! Follow along and let me know where things don't make sense or if there are errors in my thinking...

I have been interested in the ion channels, like many other MECFS researchers, for a while now. There are many threads and articles that discuss this topic but basically the ion channels are pores in the cell membrane that allow specific ions to pass through. Typical examples of these type of channels are the sodium/potassium pump which pumps out cellular waste and calcium channels.

It turns out calcium channels are pretty darn important in the proper functioning of just about everything in the body. Calcium is one of those ions that is supposed to be higher in concentration (by about 10,000x) outside of the cell in the blood and extracellular fluid. This concentration gradient is vital for the proper functioning of muscles, glial cells and neurotransmission.

Basically high intracellular calcium can cause most all the symptoms of MECFS. Fatigue, muscle recovery problems, neuroendocrine issues, mast cell issues, POTS...etc etc. (But don't worry, I'm not at all saying this is true for everyone with MECFS or that I have the cure. I'm just thinking out loud for now in the hopes that it will make sense to others too).

So it makes sense then that calcium channel blockers are sometimes helpful in symptom management in MECFS. Calcium channel blockers block (go figure) the calcium channels so that the intracellular concentration of calcium is somewhat reduced. There are several threads on this forum on that topic as well if you search for verapamil.

Verapamil is a typical calcium channel blocker and it basically reads like a wonder drug for MECFS in all the symptoms it can potentially help to correct. But so far I don't know of anyone who's been cured by verapamil unfortunately.

Calcium also affects mitochondrial function with high intracellular calcium levels causing conformational changes which make the mitochondria stop functioning well. This consequently leads to mitochondrial dysfunction but it isn't a genetic mitochondrial disorder...it's caused by the increased intracellular calcium.

Other things that seem to be helpful to us are NMDA blockers of which @Hip has a fabulous list...this is likely because the NMDA receptor also helps to indirectly lower intracellular calcium concentrations but in kind of a roundabout way.

Here's an abstract (BTW, I have all these papers if anyone wants to read them, you are welcome to PM me). This abstract talks about how NMDA antagonists and calcium channel antagonists protect against intracellular calcium increase under low oxygen conditions. Sounds pretty familiar, right?

Brain Res Bull. 2001 Mar 1;54(4):413-9.
Characteristics of protective effects of NMDA antagonist and calcium channel antagonist on ischemic calcium accumulation in rat hippocampal CA1 region.
Kubo T1, Yokoi T, Hagiwara Y, Fukumori R, Goshima Y, Misu Y.
Abstract
Effects of excitatory amino acid receptor antagonists and voltage-dependent Ca(2+) channel antagonists on ischemia-induced intracellular free Ca(2+) accumulation in rat hippocampal slices were examined. Ischemia caused a large Ca(2+) accumulation in CA1 region but a small Ca(2+) accumulation in CA3 and dentate gyrus regions. When applied during ischemia, the NMDA receptor antagonist MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine maleate) inhibited the ischemic Ca(2+) accumulation only in the CA1, but the non-NMDA receptor antagonist CNQX (6-cyano-7-nitroquinoxaline-2,3-dione) inhibited it in all the three regions. The L-type Ca(2+) channel antagonists nifedipine and verapamil inhibited the ischemic Ca(2+) accumulation only in the CA1 region, but omega-conotoxin, a N- and L-type Ca(2+) channel antagonist inhibited the Ca(2+) accumulation in all the three regions of the hippocampus. When applied after 5-min ischemia, nifedipine but not MK-801, inhibited sustained postiscehmic Ca(2+) elevation in the CA1 region but not in the CA3 and dentate gyrus regions. These findings suggest that the enhanced ischemia-induced Ca(2+) accumulation in the CA1 region is mediated via activation of both NMDA receptors and L-type-like Ca(2+) channels. It appears that sustained postischemic Ca(2+) elevation in the CA1 region is mediated via activation of L-type-like Ca(2+) channels, but not of NMDA receptors.

Turns out the hippocampus in the brain is pretty vital for MECFS patients as well.

Med Hypotheses. 2016 Jan;86:30-8. doi: 10.1016/j.mehy.2015.11.024. Epub 2015 Nov 27.
The role of the hippocampus in the pathogenesis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).
Saury JM1.

Abstract

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a severe acquired illness characterized by a profound sensation of fatigue, not ameliorated by rest and resulting in a substantial decrease in the amount and quality of occupational, social and recreational activities. Despite intense research, the aetiology and pathogenesis of ME/CFS is still unknown and no conclusive biological markers have been found. As a consequence, an accepted curative treatment is still lacking and rehabilitation programmes are not very effective, as few patients recover. Increased knowledge of the mechanisms leading to the emergence and maintenance of the illness is called for. In this study, I will put forth an alternative hypothesis to explain some of the pathologies associated with ME/CFS, by concentrating on one of the major strategic organs of the brain, the hippocampus. I will show that the ME/CFS triggering factors also impact the hippocampus, leading to neurocognitive deficits and disturbances in the regulation of the stress system and pain perception. These deficits lead to a substantial decrease in activity and to sleep disorders, which, in turn, impact the hippocampus and initiate a vicious circle of increased disability.

So that isn't the greatest article above but it does make the point that the hippocampus is pretty important for healthy functioning. @Cort makes this point as well in this article.

http://www.cortjohnson.org/blog/2015/02/16/pain-brain-hippocampal-atrophy-found-fibromyalgia/

OK, so when are we getting to the pathogen part, you ask?

It all sort of started clicking when I was reading Dr Afrin's new book on mast cell disorders (which is fascinating, BTW, and I'm only about halfway through). Mast cell disease looks to me to be a result of high intracellular calcium. And imatinib helps to lower intracellular calcium through it's action as a tyrosine kinase inhibitor. In the book, he says that he has had some success with mast cell patients with a drug called imatinib (brand name Gleevec). Imatinib is a drug primarily used in chemo to treat certain types of leukemia. It's a tyrosine kinase inhibitor.

https://www.mhealth.org/blog/2015/august-2015/struck-by-mast-cell-activation-syndrome-jennifer-credits-m-health-expert-with-saving-her-life

Although she was always very sensitive to allergens, Jennifer’s overall health began to nosedive in her early 20s. A Maryland resident, Jen was forced to resign from her job when variety of physical symptoms—including severe headaches, cognitive difficulties and fever-like problems—began to affect her health.

In 2010, Jennifer was misdiagnosed with Lyme disease. Treatment for Lyme disease did not alleviate her symptoms, which became more severe over time. Jennifer began experiencing seizure-like episodes, slurred speech, insomnia and muscle weakness.

“I was so sick and pretty much bedbound for a couple of years. My parents had to help me to the bathroom two feet away,” Jennifer said. “No doctor seemed to have any clue what was happening.”

In 2013, Jennifer was diagnosed with postural orthostatic tachycardia syndrome (POTS), which is marked by a drop in blood pressure when standing. That same year, she was also diagnosed with Ehlers-Danlos syndrome (EDS), a group of genetic disorders that primarily affect connective tissue in skin, joints and blood vessel walls.
But neither diagnosis seemed to account for all of Jennifer’s difficulties, which continued to become more severe. At times, she felt the tissues of her throat closing—a life-threatening occurrence known as anaphylaxis.
In 2013, the two doctors that diagnosed her with POTS and EDS both referred her to Lawrence Afrin, MD, who was transitioning from the Medical University of South Carolina to a new position at the University of Minnesota Medical Center. Afrin is one of the most prominent international experts on mast cell activation syndrome (MCAS).

Finally, a diagnosis and solution

When she learned Afrin was moving to the University of Minnesota, Jennifer—desperate to find a solution to her bevy of erratic and mysterious symptoms—called ahead.

In July 2014, Jennifer met with Afrin for her first appointment. After carefully examining her medical history and lab test results, Afrin told her that mast cell activation syndrome might be the “root diagnosis” to most if not all of her symptoms. Afrin ordered lab tests, but that day Jennifer’s symptoms were in remission and the tests were largely inconclusive—which is not unusual for MCAS patients.

“MCAS is a chameleon, difficult to identify for many reasons,” Afrin said. “It presents with different symptoms—which are often inflammatory or allergic in nature—to different degrees in different places in the body.” To make matters worse, many healthcare providers are not yet familiar with the condition. Though more research on MCAS is emerging, relatively little information exists about the syndrome in medical literature.

At a follow-up appointment with Afrin months later, two of Jennifer’s lab results came back positive, including her level of histamine, which was five times the normal limit. Histamine is a chemical neurotransmitter that causes allergic responses. That day, Afrin diagnosed Jennifer with mast cell activation syndrome.

Mast cells, which release histamine, are a critical component of a person’s immune system. But in patients with mast cell activation syndrome, the mast cells are over-active. Many of Jennifer’s symptoms were actually allergic reactions—caused when her hyperactive mast cells responded.

At first, Afrin prescribed a series of medication trials to try to inhibit mast cell activity, but none helped significantly. Finally, Afrin recommended a trial of a low dose of the medication Gleevec, a non-chemotherapy medication often used to treat certain blood and other cancers.

"It was Dr. Afrin who saved my life"

Within nine days of starting Gleevec, Jennifer noticed a dramatic turnaround in her health.

Gleevec prevents a key mast cell element from activating, Afrin said, and in some patients halts or reduces allergic reactions.

“I went from on death’s door step to feeling—in between my now few reactions—mostly normal,” Jennifer said. “I was able to go off twelve medications including the bottle of Benadryl [I took] a day.”

Although Jennifer still receives treatment for her conditions, she credits Afrin with tipping the scales and helping her reclaim her life. She also thanks her online support groups and her family with supporting her through her extended medical journey.

“Out of the hundreds of doctors that I have seen, it was Dr. Afrin who saved my life,” Jennifer said. “Never once did I feel the need to ‘prove’ that my symptoms were real or of physical origin as I’ve had to with other physicians. He just believed me.”
 
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Remy

Administrator
Pt 2...I've never written a post that was so long it had to be broken up!! :)

So I'm sure by now if you are still reading, your eyes are rolling back into your head and glazing over so I'm going to be short and simple here as much as possible.

There's this protein called Tat that they have discovered in HIV-1 infected brain cells. Basically this protein causes high intracellular calcium and glutamate excitotoxicity which leads to cell death and dementia in HIV positive patients. Glutamate is another excitatory neurotransmitter that has been studied and studied in MECFS because it often is elevated and causes neurological sensitivity problems to sound and light in particular.

J Neurochem. 2001 Aug;78(3):457-67.
HIV-1 Tat through phosphorylation of NMDA receptors potentiates glutamate excitotoxicity.

Haughey NJ1, Nath A, Mattson MP, Slevin JT, Geiger JD.
  • 1Laboratory of Neurosciences, National Institute on Aging, Baltimore, Maryland, USA.
Abstract

Toxic effects of HIV-1 proteins contribute to altered function and decreased survival of select populations of neurons in HIV-1-infected brain. One such HIV-1 protein, Tat, can activate calcium release from IP3-sensitive intracellular pools, induce calcium influx in neural cells, and, as a result, can increase neuronal cell death. Here, we provide evidence that Tat potentiates excitatory amino acid (glutamate and NMDA) triggered calcium flux, as well as glutamate- and staurosporine-mediated neurotoxicity. Calcium flux in cultured rat hippocampal neurons triggered by the transient application of glutamate or NMDA was facilitated by pre-exposure to Tat. Facilitation of glutamate-triggered calcium flux by Tat was prevented by inhibitors of ADP-ribosylation of G(i)/G(o) proteins (pertussis toxin), protein kinase C (H7 and bisindolymide), and IP3-mediated calcium release (xestospongin C), but was not prevented by an activator of G(s) (cholera toxin) or an inhibitor of protein kinase A (H89). Facilitation of NMDA-triggered calcium flux by Tat was reversed by inhibitors of tyrosine kinase (genestein and herbimycin A) and by an inhibitor of NMDA receptor function (zinc). Tat increased 32P incorporation into NMDA receptor subunits NR2A and NR2B and this effect was blocked by genestein. Subtoxic concentrations of Tat combined with subtoxic concentrations of glutamate or staurosporine increased neuronal cell death significantly. Together, these findings suggest that NMDA receptors play an important role in Tat neurotoxicity and the mechanisms identified may provide additional therapeutic targets for the treatment of HIV-1 associated dementia.
Many of us are familiar with how typical antiviral drugs work as thymidine kinase inhibitors. These are different types of proteins but it turns out that they are related and some antivirals act as both thymidine and tyrosine kinase inhibitors.

It makes a lot more sense that AVs are helping some of us by means other than killing viruses. AVs are very slow at killing viruses. To kill the reservoir of EBV in a person with typical doses of AVs, it would take on the magnitude of decades. So obviously something else is helping the people that see great improvement with AVs. Is it immunomodulatory because these drugs are able to help lower intracellular calcium too?

So is it likely that HIV is the *only* virus that produces a Tat (or Tat-like) protein that can cause these effects in the brain? I find that scenario highly, highly unlikely.

Here they studied tyrosine kinase inhibitors on herpes simplex 1...and found increased viral suppression up to 82.4% vs the control. I don't know about you but 82.4% seems like quite a high number to me!

Intervirology. 1997;40(1):7-14.
Effects of protein tyrosine kinase inhibitors on the replication of herpes simplex virus and the phosphorylation of viral proteins.

Yura Y1, Kusaka J, Tsujimoto H, Yoshioka Y, Yoshida H, Sato M.
Abstract
The effect of protein tyrosine kinase (PTK) inhibitors on the replication of herpes simplex virus (HSV) was examined. Tyrphostins AG17, AG213, AG490, and AG555, and herbimycin A all inhibited the plaque formation of HSV type 1 (HSV-1) in Vero cells, but AG17, AG490, and AG555 exhibited a more selective antiviral effect. In the presence of 0.4 microM AG17, the virus production 24 h after infection was decreased to 7.7% of the untreated control level. Even if the treatment was started 12 h after the initiation of infection, the viral titer was reduced by 82.4%, compared with the untreated control level. In HSV-1-infected cells ICPs 6, 17/18, 19/20, and 25 were tyrosine-phosphorylated proteins. The synthesis and phosphorylation of these proteins were inhibited by AG17, and suppression of ICP 19/20, which were identified as the UL47 gene products, was the greatest. In contrast, the in vitro autophosphorylation of viral proteins was not affected by this PTK inhibitor. These results indicate that tyrphostin may represent a novel class of inhibitors of HSV-1, and that the viral proteins which have phosphorylated tyrosine residues and are suppressed by AG17 most significantly are the products of the UL47 gene, the tegument proteins VP13/14.
So there's my theory in a nutshell...viruses can code for proteins like a Tat protein which cause the calcium channels to go beserk. High intracellular calcium can cause basically any and every system in the body to malfunction which may go some ways to explaining why there is overlap in symptoms but every one of us has a somewhat unique presentation of the disease and responds better or worse to the same interventions due to our own genetic makeup.

So what's the answer? Get the calcium out of the cell and let the mitochondria work properly again and the brain work properly again and the metabolism work properly again...and get well. Has anyone ever studied this? Calcium influx is supposed to be transiently high and then low again as the channel resets itself. Persistently increased calcium levels should tell us something!

FWIW, I also think it's possible that there could be an autoimmune variation to this with antibodies against the calcium channel but I haven't gotten very far at all down that road...yet.

I've left so much out. But I've already written a book. What do you all think?
 

Who Me?

Well-Known Member
You know I don't get science (ME brain) but I was able to understand most of this (remember is another thing). Thanks for citing where you got your information and that this is you just thinking out loud vs. pronouncing it is a cure.

My NP has talked about the Mitochondria and fixing that. I have an appointment in 2 weeks so I'm going to bring up the verapamil with her. My only thought, and again, I'm clueless about the science how a CCB affects BP if your BP is normal.

@Upgrayedd This might interest you.
 

Remy

Administrator
how a CCB affects BP if your BP is normal.
The doses used for things like autism seem to be much lower than what are used for hypertension. So that should help. And like I said, verapamil doesn't seem to be the total answer though it does seem to provide symptom relief for some in some areas.

I took it for a week before I had to stop due to interactions with diflucan and did not notice any effect on my BP which is normal to low-normal typically.

This blog on verapamil use was enlightening to me...

http://epiphanyasd.blogspot.com/2014/07/verapamil-for-broader-sub-group-of.html

It's also interesting to note that verapamil is being studied at UAB (the home of our friend Dr Younger) as a potential way to reverse (ie cure) diabetes.
 

Upgrayedd

Active Member
I'll be following up with my Cardiologist soon, and it looks like I'm headed towards BP medicine anyway, so I will be asking him to consider a calcium channel blocker, maybe Verapamil. One of the CFS gurus, either Goldstein or Cheney used Nimotipine, which is another calcium channel blocker, although it seems to target the brain more than the heart.
 

Remy

Administrator
I have tried verapamil and unfortunately it made my symptoms much, much more worse!!!
If Dr Afrin's work is anything to go by, finding the medication that works for a patient is still a difficult job. Things that work brilliantly for one person will fail miserably for the next for as of yet unknown reasons.

Verapamil isn't going to be the cure and it will for sure make some people unfortunately worse just like any other med.

But that doesn't mean that high intracellular calcium caused by an exposure to a pathogenic virus of some sort couldn't still be at the heart of this disorder.
 

Wayne

Well-Known Member
I've left so much out. But I've already written a book. What do you all think?
Hi Remy,

Very interesting reading Remy -- I think I very much appreciate the time and effort you put into writing a book for us! :)

I'm mostly focusing on nutritional deficiencies these days, and how they can impact our health in so many ways. The three that have helped me the most in the past few weeks have been iodine, magnesium chloride, and niacin. The latter two especially seem to have been instrumental in settling down my neurological system to a degree I've not experienced for quite some time. The common experience of many with ME/CFS of "tired but wired" has improved considerably for me.

It seems that whenever there's a discussion on calcium, it ties into its relationship with magnesium, and vice versa. So maybe some of the symptom improvement I'm experiencing ties into some of your theories and observations on calcium. I think the niacin part is more prominent at this time however.

I'm currently reading a book on niacin, and how it's been used to treat pellagra and other conditions resembling it. "Mental conditions" such as schizophrenia, depression, etc. that resemble the "mental conditions" of pellagra have been helped immensely using high doses of niacin to correct metabolic deficiencies.

One of the most notable sentences in the book I'm reading went something like, "Thousands of schizophrenics have recovered from using niacin therapy". Could high niacin intake successfully treat some of the cognitive and other issues that are so common in ME/CFS? My best guess is yes.

So much left out... I've not yet written a book, but I think that's about all the energy I have for some of my random thoughts for today. Always appreicate your posts Remy. :)

Best, Wayne
 

weyland

Well-Known Member
Most of this stuff is way over my head and it's hard to talk about this generally because there are hundreds of different types of ion channels in our body. If the problem is excessive intracellular calcium then I'm not sure it's necessarily a problem with the ion channels though. It seems like it would be more of a problem with the calcium pump that removes intracellular calcium after the influx through the ion channel. These pumps of course run on ATP and given our metabolic issues it wouldn't be too surprising if these pumps weren't working optimally.

Other things that seem to be helpful to us are NMDA blockers of which @Hip has a fabulous list...this is likely because the NMDA receptor also helps to indirectly lower intracellular calcium concentrations but in kind of a roundabout way.
As is always the problem with these drugs, it's hard to know why something is helping. I've had improvement from taking amantadine, which is an NMDA antagonist, but it's also a translation inhibitor against enterovirus. It's probably impossible to know by which mechanism it's helping.
 

Upgrayedd

Active Member
From wiki @Upgrayedd

Nimodipine (marketed by Bayer as Nimotop) is a dihydropyridinecalcium channel blockeroriginally developed for the treatment of high blood pressure. It is not frequently used for this indication, but has shown good results in preventing a major complication of subarachnoid hemorrhage (a form of cerebral hemorrhage) termed vasospasm; this is now the main use of nimodipine.
Thanks. I've read similar data on Nimotop. It's because it's effects target the brain, rather than the heart, that it may have some off label usefulness with CFS/ME patients. On the other hand, it is not the most effective med for lowering overall blood pressure. As you noted, they use it for patients with damage to the brain (like you and me!)
 

Remy

Administrator
One of the most notable sentences in the book I'm reading went something like, "Thousands of schizophrenics have recovered from using niacin therapy". Could high niacin intake successfully treat some of the cognitive and other issues that are so common in ME/CFS? My best guess is yes.
Niacin increases prostaglandin levels which are almost always high in MCAD.

And this article says that prostaglandins sensitize the calcium channel, causing two to fourfold increases in the calcium current.
 

Remy

Administrator
If the problem is excessive intracellular calcium then I'm not sure it's necessarily a problem with the ion channels though.
It's not a problem with the ion channels per se.

It's a problem (maybe!) caused by a pathogen-produced protein that opens the calcium channel that results in higher than normal levels of intracellular calcium which then causes a myriad of other problems.

The reason we have a loss of ATP is due to the mitochondrial changes caused by the high intracellular calcium. It becomes a self-propagating loop.

Gee, maybe I should summarize myself more often. :D:wacky: That was sure a lot shorter than my first two posts!
 

Who Me?

Well-Known Member
Thanks. I've read similar data on Nimotop. It's because it's effects target the brain, rather than the heart, that it may have some off label usefulness with CFS/ME patients. On the other hand, it is not the most effective med for lowering overall blood pressure. As you noted, they use it for patients with damage to the brain (like you and me!)
You can be the guinea pig on this one. And get a free T-Shirt!!
 

Remy

Administrator
This theory could even potentially explain why women are at increased prevalence and risk. It turns out estrogen increases intracellular calcium.


J Lab Clin Med. 1993 Mar;121(3):486-92.
Red blood cell calcium level is elevated in women: enhanced calcium influx by estrogens.
Gafter U1, Malachi T, Barak H, Levi J.
Author information

Abstract

Red blood cell (RBC) calcium level had been found to be higher in women than in men. This study was designed to evaluate whether this is a general phenomenon and to elucidate a possible mechanism for a gender-related difference in RBC calcium levels. Differences in RBC calcium levels between women and men were examined in normal subjects, in patients with chronic renal failure (CRF) who were known to have elevated RBC calcium levels, and in female and male rats. RBC calcium level was higher in healthy women (6.1 +/- 0.5 mumol/L in women vs 4.4 +/- 0.3 mumol/L in men; p < 0.01), in women with CRF (45.8 +/- 11.8 mumol/L vs 15.4 +/- 1.1 mumol/L in men with CRF; p < 0.025) and women undergoing hemodialysis treatment (43.4 +/- 4.7 mumol/L vs 8.8 +/- 0.9 mumol/L in men undergoing hemodialysis p < 0.001). RBC calcium levels in female rats were also significantly higher than those in male rats. Ovariectomy reduced RBC calcium levels in female rats to those of male rats, whereas castration of male rats had no effect on RBC calcium levels. These in vivo findings suggest that the elevated RBC calcium level is associated with activity of female sex hormones. To investigate a possible mechanism, the in vitro effect of beta-estradiol on calcium 45 influx into RBCs and its effect on basal and calmodulin-stimulated Ca adenosine triphosphatase (CaATPase) activity in RBC membranes was determined. CaATPase activity was not affected by beta-estradiol at various concentrations and different incubation periods.(ABSTRACT TRUNCATED AT 250 WORDS)
 

Justin

Active Member
Two points Dr Goldstein pointed out Ketamine as one of his top treatments as it deals directly on the NMDA Receptor.

Chenney pointed out Klonopin for the NMDA Receptor. Mag and taurine were also implicated as well.

I have to use the later 2 or I dont think I would have any life.

What really needs to happen in my eyes is to determine if permanent damage has been inflicted on the brain through PET and SPECT Scans and better MRI's.

The reality is that when you look at true ME....as per Ramsay and you compare with the symptoms with people who had encephalitis and other types of encephalomylietis there is major overlapp.

Further some seem to have a a direct insult to the immune system instead the ones that get a ton of flu like symptoms.

Others get the combo shot. Immune and nervous system.

Others have persitent infections infections that were never picked up...

Then others get completely misdiagnosed.....they have an Autoimmune Disease, rare genetic disorder, rare neurologic disorder, rare immune disorder, etc.....

Others have true encephalitis or encephalomylietis that was undiagnosed and untreated at onset.....this one really bugs me because I have a hunch that government and health authorities dont want to admit that through lack of adequate testing for millions around the world they were not able to diagnose the encephalopathy that is caused by so many viruses, bacterias, vaccines and fungi at onset.

Bottom line is that they need to start attracting and getting a lot of people involved and excited to research and define the disease. Which is happening.....
 

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